The Clinical Profile and Pathophysiology of Atrial Fibrillation Relationships Among Clinical Features, Epidemiology, and Mechanisms
The Clinical Profile and Pathophysiology of Atrial Fibrillation Relationships Among Clinical Features, Epidemiology, and Mechanisms
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DOI：
10.1161/circresaha.114.303211
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发表时间：
2014-04-25
影响因子：
20.1
通讯作者：
Nattel, Stanley
中科院分区：
文献类型：
--
作者：
Andrade, Jason;Khairy, Paul;Nattel, Stanley
房颤（AF）是最常见的心律失常（估计终生风险为22%-26%）。本文的目的是回顾房颤的临床流行病学特征，并将其与潜在机制联系起来。长期确定的房颤风险因素包括老龄化、男性、高血压、瓣膜疾病、左心室功能障碍、肥胖和饮酒。新出现的危险因素包括高血压前期、脉压增加、阻塞性睡眠呼吸暂停、高水平体育训练、舒张功能障碍、易感基因变异、肥厚型心肌病和先天性心脏病。潜在的风险因素包括冠状动脉疾病、肾脏疾病、全身炎症、心包脂肪和吸烟。AF对人群健康有重大影响，包括生活质量受损、住院率增加、卒中发生率和医疗费用增加。房颤的病理生理学主要围绕4种促进异位放电和折返机制的一般类型的紊乱，包括：（1）离子通道功能障碍，（2）Ca 2+处理异常，（3）结构重塑和（4）自主神经调节障碍。衰老、高血压、瓣膜病、心力衰竭、心肌梗死、肥胖、吸烟、糖尿病、甲状腺功能障碍和耐力运动训练都可引起结构重塑。心力衰竭和既往心房梗死也可引起Ca 2+处理异常，通过延迟后除极/触发活动导致局灶性异位放电。神经失调是与耐力运动训练和闭塞性冠状动脉疾病相关的房性心律失常发生的核心。房颤的单基因病因通常通过离子通道功能障碍促进心律失常，但更常见的多基因危险因素的机制仍然知之甚少，并正在进行深入研究。需要更好地认识房颤的临床流行病学，以及更好地理解潜在机制，以开发更好的房颤预防和管理方法。
Atrial fibrillation (AF) is the most common arrhythmia (estimated lifetime risk, 22%-26%). The aim of this article is to review the clinical epidemiological features of AF and to relate them to underlying mechanisms. Long-established risk factors for AF include aging, male sex, hypertension, valve disease, left ventricular dysfunction, obesity, and alcohol consumption. Emerging risk factors include prehypertension, increased pulse pressure, obstructive sleep apnea, high-level physical training, diastolic dysfunction, predisposing gene variants, hypertrophic cardiomyopathy, and congenital heart disease. Potential risk factors are coronary artery disease, kidney disease, systemic inflammation, pericardial fat, and tobacco use. AF has substantial population health consequences, including impaired quality of life, increased hospitalization rates, stroke occurrence, and increased medical costs. The pathophysiology of AF centers around 4 general types of disturbances that promote ectopic firing and reentrant mechanisms, and include the following: (1) ion channel dysfunction, (2) Ca2+-handling abnormalities, (3) structural remodeling, and (4) autonomic neural dysregulation. Aging, hypertension, valve disease, heart failure, myocardial infarction, obesity, smoking, diabetes mellitus, thyroid dysfunction, and endurance exercise training all cause structural remodeling. Heart failure and prior atrial infarction also cause Ca2+-handling abnormalities that lead to focal ectopic firing via delayed afterdepolarizations/triggered activity. Neural dysregulation is central to atrial arrhythmogenesis associated with endurance exercise training and occlusive coronary artery disease. Monogenic causes of AF typically promote the arrhythmia via ion channel dysfunction, but the mechanisms of the more common polygenic risk factors are still poorly understood and under intense investigation. Better recognition of the clinical epidemiology of AF, as well as an improved appreciation of the underlying mechanisms, is needed to develop improved methods for AF prevention and management.